title: Therapeutic benefit of Yangxue Qingnao Granule on cognitive impairment induced by chronic cerebral hypoperfusion in rats.
abstract: OBJECTIVE
  To observe the therapeutic effect of Yangxue Qingnao Granule (, YXQNG) on cognitive impairment induced by chronic cerebral hypoperfusion and to investigate its impact on oxidative stress, apoptosis, and the cholinergic system.
  
  
  METHODS
  Adult male Wistar rats were subjected to chronic cerebral hypoperfusion by permanent occlusion of bilateral common carotid arteries (2-VO). Thirty rats were randomly assigned to one of the five treatment groups in a 1:1:1:1:1 ratio: sham operation plus normal saline treatment, 2-VO plus normal saline treatment, 2-VO plus YXQNG at a dose of 2 g·kg(-1)·d(-1) or 4 g·kg(-1)·d(-1), or 2-VO plus rivastigmine 2 mg·kg(-1)·d(-1). The Morris water maze test was used to assess the spatial memory retrieval. Apoptosis, total antioxide capacity (T-AOC), acetylcholine esterase (AchE) and choline acetyl transferase (ChAT) activities in the hippocampus and the cortex were investigated.
  
  
  RESULTS
  In the chronic cerebral hypoperfusion model, the 2-VO plus saline treatment resulted in impaired special learning as shown by the significantly prolonged escape latency and shorter swim time in the first quadrant as compared to the sham operation. The impairment was associated with apoptosis and significant decreases in T-AOC, AchE and ChAT activities in the hippocampus and the cortex. Treatment with YXQNG at either 2 g·kg(-1)·d(-1) or 4 g·kg(-1)·d(-1) dose, or rivastigmine resulted in significantly shorter escape latencies and longer swim time in the first quadrant. YXQNG at both doses, but not rivastigmine, had significant reduction in apoptosis, and significant increases in T-AOC and ChAT activity in both the hippocampus and the cortex. Unlike rivastigmine, neither dose of YXQNG showed significant reduction in AchE activity.
  
  
  CONCLUSIONS
  YXQNG ameliorated cognitive impairment induced by chronic cerebral hypoperfusion. The protective effect may be mediated through its regulation of apoptosis and activities of T-AOC and ChAT in the hippocampus and cortex of the rats in the chronic cerebral hypoperfusion model, a mechanism that is different from rivastigmine.
authors.affiliation: Department of Neurology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
authors.forename: Li
authors.initials: L
authors.lastname: Xiong
authors.forename: Jun-Jian
authors.initials: JJ
authors.lastname: Zhang
authors.forename: Dong
authors.initials: D
authors.lastname: Sun
authors.forename: Hui
authors.initials: H
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000473:pathology; D002626:Chemistry, Pharmaceutical; D002908:Chronic Disease; D003072:Cognition Disorders / Q000188:drug therapy* / Q000209:etiology* / Q000473:pathology; D004195:Disease Models, Animal; D004353:Drug Evaluation, Preclinical; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage / Q000627:therapeutic use*; D020925:Hypoxia-Ischemia, Brain / Q000150:complications* / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013037:Spatial Behavior / Q000187:drug effects; D013647:Task Performance and Analysis
chemical_list: D004365:Drugs, Chinese Herbal